- In type 2 diabetes, the quantities of insulin the body produces to regulate blood sugar levels are insufficient.
- A new lab-based study suggests a surprising role of fat in maintaining insulin production by the pancreas in conditions of excess sugar.
- A cycle of fat storage and mobilization in the pancreas may preserve the organ’s ability to make insulin.
- The finding could explain how intermittent fasting might help prevent and treat type 2 diabetes.
In diabetes, this regulatory mechanism starts to break down either when the pancreas fails to produce enough insulin or when the body’s tissues become resistant to the hormone’s effects.
According to the
Scientists have reached a consensus that high blood sugar levels damage beta cells in the pancreas — the cells that make insulin — but the part that fat plays is more controversial.
Findings from a new lab-based study suggest that fat stores in the pancreas may help maintain insulin secretion and slow the onset of diabetes.
The study indicates that a cycle of fat storage in pancreas cells after mealtimes, followed by the breakdown of fat in the hours before the next meal, may help maintain insulin production.
The research, led by scientists at the University of Geneva Medical Centre in Switzerland, appears in the journal Diabetologia.
The scientists exposed human and rat beta cells to periods of excess sugar, with or without high fat levels.
As expected, over time, high sugar levels reduced the cells’ ability to secrete insulin, compared with normal sugar levels.
However, an abundant supply of fat appeared to protect the beta cells’ insulin secretion against the effects of high sugar levels.
“When cells are exposed to both too much sugar and too much fat, they store the fat in the form of droplets in anticipation of less prosperous times,” Lucie Oberhauser, Ph.D., first author of the study, explains.
“Surprisingly, we have shown that this stock of fat, instead of worsening the situation, allows insulin secretion to be restored to near-normal levels,” she adds.
The researchers observed that periods of high fat and sugar availability, alternating with low availability, activated genes in pancreatic cells that promoted a cycle of fat storage and mobilization.
The benefits of this cycle became apparent during periods when the cells no longer had ample energy supplies.
“These fasting-like conditions induced fat mobilization that supported insulin secretion,” said Pierre Maechler, Ph.D., who led the study.
“In other words, the whole cycle of fat storage (overnutrition) followed by fat mobilization (fasting) is required for the mechanism uncovered in our study,” he told Medical News Today.
He said a fast of just 4–6 hours would be sufficient to allow beta cells to reset and recover their insulin-secreting capacity between meals.
“Practically, avoid snacking!” he advised.
He believes that the release of fat from stores is not a problem provided the body uses it as a source of energy between mealtimes — for example, to fuel regular bouts of physical activity.
Other scientists have questioned whether these findings from isolated pancreas cells growing in dishes in a lab can be extrapolated to people with obesity.
“[I]n truth, the higher the [body mass index], the higher the risk of diabetes, and there is evidence that excess fat deposition in key organs, such as [the] liver and pancreas, accelerates diabetes risks,” said Naveed Sattar, Ph.D., professor of metabolic medicine at the University of Glasgow in the United Kingdom.
“There is plentiful evidence high circulating triglycerides, which deliver excess fat to [the] pancreas, may accelerate diabetes risk,” he told MNT.
Triglycerides are a type of fat that the body uses as fuel.
Prof. Sattar cited a
The Diabetes Remission Clinical Trial shows that when people recover from diabetes as a result of weight loss, their long-term remission depends on continuing low levels of triglycerides in their bloodstream and low levels of fat in their pancreas.
Dr. Francesco Rubino, chair of Metabolic and Bariatric Surgery at King’s College London in the U.K., also cautioned that the new lab-based study may not reflect what happens in the body.
He told the Science Media Centre (SMC) in London that type 2 diabetes involves problems with other tissues and organs, not just the pancreas. For example, experts associate excess fat with widespread insulin resistance and inflammation.
“Hence, it is difficult to assess the clinical relevance of the observations from this study and, specifically, the potential role of fat as ‘protective’ for the development of diabetes as suggested by the authors,” he said.
However, he pointed out that, while the association between excess fat and diabetes is clear, the nature of the association is less obvious.
Katarina Kos, M.D., Ph.D., senior lecturer and honorary consultant physician in diabetes and endocrinology at the University of Exeter Medical School in the U.K., told the SMC:
“It would be wrong to take from this study that fat rescues the pancreatic insulin-secreting cell once damaged. Reduced nutritional intake combined with exercise improves insulin sensitivity, and this remains the key recommendation for prevention and treatment of type 2 diabetes.”